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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3803_Библиотеки_им_академика_М_И_Перельмана
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lipid- rich cells, apoptotic macrophages, amorphous debris and matrix bre remnants [9]. That cap may thicken and calcify the intima over time creating the
appearance of plaque calcication during procedural imaging [10]. Concurrently,
the necrotic core may enlarge causing luminal reduction and stenosis. Advanced
plaque expansion which involves a signicant proportion of the blood vessel circumference and the associated calcication is known to reduce elasticity and
compliance [11].
Calcication of the media layer occurs with ageing and is associated with chronic
kidney disease (CKD) and diabetes mellitus [12, 13]. It is independent of atherosclerosis, despite the two processes commonly occurring together as they have similar risk factors [14]. The process begins when hydroxyapatite crystals are deposited
on to degraded elastin bres inciting an osteoblast-like differentiation of the adjacent vascular smooth muscle cells (VSMC) [15]. This VSMC differentiation is also
observed as part of normal ageing and the increased oxidative stress which may
occur with CKD, smoking and diabetes [16].
It is common for atherosclerotic plaque stenosis to require angioplasty revascularisation in the context of coexisting blood vessel wall calcication and reduced
compliance. Dissection is a frequent complication, with the potential to limit the
durability of that procedure.
A. Stathis et al.
Barotrauma andtheImmediate Cellular Response
toAngioplasty
Percutaneous transluminal angioplasty (PTA) uses high-pressure expansion to dilate
the stenotic plaque and achieve luminal gain. During ination, the intima, media
and adventitia are mechanically stretched by the outward force exerted from the
balloon [17, 18]. With low-pressure ination, the inherent elastic properties of the
blood vessel (compliance) allow it to return to the original luminal diameter when
the balloon deates [18, 19]. However, with high pressure and increased stretch, the
elastic properties of the artery are overcome, cleaving the intima and often media
[19, 20]. These disrupted layers of blood vessel wall heal and remodel, ultimately
facilitating an increased luminal diameter which restores blood supply to the
extremity [18, 20].
It is important for angioplasty to disrupt the atherosclerotic plaque and the
elastic properties of the inner layers of arterial wall if it is to result in permanent
remodeling [18, 21]. This involves a physical trauma at the plaque-artery interface, stretching and tearing of the endothelium and alteration of the blood vessel
substructure [20]. With that angioplasty-induced barotrauma come denudation
of the endothelium and the immediate release of thrombogenic and vasoactive
factors which promote platelet aggregation, thrombus formation and inammation [22, 23]. Damage at the media level results in the necrosis of VSMC and
matrix bres, macrophage activation and release of cytokines and growth factors
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[23]. This triggers a cascade response which ultimately results in the migration
of VSMC from the media to intima, where they proliferate, undergo metaplasia
and produce additional extracellular matrix [23, 24]. This process, and the cellular/matrix lesion which results, is called neointimal hyperplasia (NIH). In its
early stages, it is considered a healthy response which facilitates blood vessel
healing.
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Mid-Term Cellular Response andRemodeling
Vascular remodeling can be described as negative (luminal reduction) or positive
(luminal enlargement) [25, 26] and under normal conditions relies on an intact
endothelium. Glagov etal. were the rst to demonstrate that human coronary arteries undergo compensatory positive remodeling in response to decreased blood ow
[26], with the same mechanism now also described in peripheral vessels [27].
However, angioplasty trauma mediated through cytokine and chemokine release
may also lead to tissue remodeling and structural change. Normally, the intact endothelial layer inhibits platelet aggregation; however, angioplasty-induced barotrauma
damages and denudes that inner layer of cells with an immediate release of thrombogenic and vasoactive factors that promote platelet aggregation and localised
inammation [23]. The degranulation of platelets releases chemokines and cytokines that lead to the migration and proliferation of VSMC located in the media.
Furthermore, if the angioplasty trauma leads to stretching and tearing of the media,
it may result inlocalised VSMC necrosis and release of additional growth factors.
Together, these trigger a complex interaction between VSMC, platelets, endothelial
cells, leukocytes and cellular mediators that culminate in remodeling and formation
of neointimal hyperplasia (NIH) [24]. The mitogenic substances released by the
degranulating platelet plug, together with those by the damaged media, result in the
migration of VSMC from the media to intima. A signicant proportion of those
migratory VSMC proliferate and form new extracellular matrix (ECM) within the
neointima [28]. If over- exuberant, NIH can lead to a pathophysiological compromise of the lumen, a description synonymous with negative remodeling which may
lead to restenosis and the return of ischemic symptoms.
In addition to migration and proliferation of VSMC, there is evidence to suggest
the barotrauma from angioplasty results in permanent functional change of the
endothelium. It is known that regions of chronic denudation feature a layer of bronectin, which can prevent the regrowth of endothelial cells [24, 29]. The increased
production of the extracellular matrix protein bronectin is driven by the release of
transforming growth factor β1 (TGF- β1) from aggregated platelets [24, 29–31].
This process highlights the impact of the ECM on endothelial recovery following
balloon angioplasty. In regions where the endothelium has recovered, the presence
of actin stress laments within them suggests that those overlying the NIH are operating in an altered functional state [32].
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A1
B1
Intima Media Calcified plaqueAdventitia
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A. Stathis et al.
The Concept ofControlled Versus Uncontrolled Dissection
The goal of PTA is to create a series of small, controlled, blood vessel wall dissections that facilitate permanent luminal gain by enabling radial expansion [18] while
avoiding large, ow-limiting dissections that might result in acute occlusion or lead
to restenosis (Fig.5.1) [19]. Histopathology studies demonstrate that microdissection and arterial wall disruption occur to some degree after every angioplasty [17,
33, 34]. However, there are aspects of the individual disease and procedural tech-
nique that can help predict the likelihood of uncontrolled dissection which may
have detrimental clinical consequences. The nature of the atherosclerotic plaque
may inuence the angioplasty result and type of dissection observed. Calcied
lesions are less compliant and more susceptible to dissection, even at lower force
[20, 35]. Circumferential plaque is thought to evenly distribute the forces of angioplasty, resulting in small fractures and dissections at the thinner portions of the
plaque [17, 20, 35], whereas eccentric lesions are more likely to dissect entirely
from the blood vessel wall and at the margin of plaque and the normal underlying
media [22]. Angioplasty of calcied vessels may result in cleavage of the plaque,
putting the underlying vessel under high stress and increasing the risk of signicant
intimal dissection [20]. Moreover, sections of non-compliant artery may disproportionately transfer the angioplasty force in a proximal and distal direction causing
stretch and increasing the risk of uncontrolled dissection in those adjacent zones
[20, 35]. Angioplasty techniques used during treatment may also play a role.
A2 A3
B2 B3
Fig. 5.1 Controlled and uncontrolled dissection. Controlled dissection induced by balloon angioplasty (A1–A3). A2 demonstrates the microdissections which result from balloon ination (black
arrows) and A3 the nal result with circumferential dilatation of the luminal area (A3). Uncontrolled
dissection (B1–B3) with calcied plaque in the intimal layer (grey shaded area), balloon ination
transfers shearing force to the plaque edge (B2, white arrows) leading to uncontrolled macrodissection which may have negative clinical consequences (B3, white arrows)
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Subintimal wire passage prior to balloon ination and the use of adjunctive atherectomy are two procedural aspects known to increase the risk of dissection [36],
whereas prolonged angioplasty ination times and the use of long (versus multiple
short) balloon lengths are known to reduce it [37–39].
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Stents forMechanical Support
Nitinol self-expanding bare metal stents were developed to overcome some of the
limitations observed with PTA.By providing mechanical scaffolding, they stabilise
the treated blood vessel segment and overcome elastic recoil by exerting ongoing
force on the vessel wall. However, that same chronic outward force results in a
chronic low-grade vascular injury which can lead to the development of NIH deposited between the stent interstices. This NIH may also limit the durability of any
stent-based intervention. A next generation of nitinol stents coated in antiproliferative drugs such as paclitaxel have been developed to limit the NIH response and
reduce the incidence of in-stent restenosis. They have been shown to be superior to
PTA and bare metal stents in multiple randomised trials [40, 41].
Modes ofFailure Following Balloon Angioplasty
As described, angioplasty-induced barotrauma leads to a cellular response, and the
blood vessel remodeling which follows can result in acute or delayed target lesion
restenosis/failure. Uncontrolled macrodissection can also lead to poor clinical outcomes. Those may also occur in the acute setting within 24h of PTA or take the
form of a recurrent stenosis weeks or months after the index procedure.
Acute Occlusion
Acute occlusion occurs during or immediately after (<24h) an angioplasty procedure. It is caused by mechanical obstruction which may result from any combination of occlusive dissection, thrombus formation, intraplaque haemorrhage,
vasospasm and elastic recoil [42]. In practice, it is difcult to distinguish between
these multiple mechanical factors, and it is common for there to be signicant overlap. However, intravascular imaging with ultrasound or optical coherence tomography may be useful to determine the dominant mechanism.
Hypercoagulability factors are also known to play a role [43]. These range from
the disruption of plaque contents which leads to tissue factors within the lipid core
encountering the circulating blood to inadequate intra-procedural heparinisation.
There are also a group of patients who are resistant to heparin and/or antiplatelet
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agents making them more susceptible to thrombus formation, even with correct dosage administration [44, 45].
A dissection which results in pressurised blood ow into the false lumen may
propagate, spiral, compromise the true lumen and result in complete obstruction of
ow. Stents and tack devices may be useful to treat ow-limiting dissection and
overcome elastic recoil. However, they are not without their own limitations. The
introduction of a foreign body into the circulation may result in platelet aggregation
and thrombus formation unless antiplatelet agents are used and they remain vulnerable to metal fatigue-related fracture [46, 47].
A. Stathis et al.
Restenosis
It is well established that the barotrauma exerted on the blood vessel wall by an
inated angioplasty balloon may lead to negative remodeling and recurrent stenosis
[23]. It is also a common view amongst peripheral interventionalists that dissection
itself is a predictor of negative remodeling and target lesion failure [48]. It is uncertain whether the dissection is a marker for more advanced patterns of disease leading
to reduced vessel compliance which predisposes to both the dissection and progressive disease or whether the dissection itself triggers a more exuberant form of NIH
and elastic recoil that results in that recurrent stenosis. In the coronary literature,
angiographic dissection has been classied and found to be associated with worse
clinical outcomes [49, 50]. While it is known that physicians are more likely to
implant stents with more severe forms of dissection, we know less about whether
peripheral artery dissections lead to early restenosis and loss of patency [51, 52]. One
observational study by Kobayashi etal. divided dissection types into 3 groups (A, no
dissection; B, mild dissection; C, severe dissection) and followed 319 patients longitudinally after undergoing PTA for femoropopliteal disease. They found that 3-year
primary patency was signicantly reduced in those patients with severe dissection,
but not mild (66.0% in group A, 63.8% in group B and 32.5% in group C; p<0.001).
This nding was more pronounced in longer length disease which was another independent predictor of reduced patency. They recommended that stents were not
required for mild and short dissections, but that they continue to be used for severe
dissection, particularly over longer lengths. Another study by Fujihara etal. used the
NHLBI angiographic grading system to evaluate outcomes in 621 patients being
treated for de novo disease of the supercial femoral artery [52]. They found that
severe dissection was a signicant risk factor for restenosis, which rose progressively
from types C to F, and that after 2-year follow-up, the severe dissection group (types
C–F) showed a signicantly lower patency rate (p < 0.001) and higher clinically
driven TLR (p<0.001) compared to the non-severe group (no dissection and type
A–B dissection). Together, these studies support the view of many experts in the eld
that severe dissection is a predictor of early restenosis and target lesion failure.
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The Classication ofDissection
A detailed classication of angioplasty-induced dissection is helpful to provide
uniform consistency in reporting and use in clinical trials and to guide discussion
around treatment. Several classication systems have been proposed, many of
which have been developed as tools to guide coronary interventions. Translation
to a peripheral artery application is feasible as most systems can be made to
apply to both arterial regions. However, experts disagree as to the relevance of
some coronary dissection characteristics to peripheral arteries which have several distinct and important differences. Herein, we discuss the systems in
common use.
Classication Systems: Angiography
The National Heart, Lung, and Blood Institute Percutaneous Transluminal Coronary
Angioplasty (NHLBI PTCA) Registry published its manual of operations in 1985,
describing the morphological presentations of arterial dissections that occur during
percutaneous coronary interventions [53]. In the mid-1980s, cine-loop uoroscopy
was the dominant imaging modality used to diagnose and classify dissections, with
less availability of intravascular ultrasound. The classication system developed by
the NHLBI reected that period. It distinguished six categories ranging from simple
linear to spiral morphologies (A–F). It included contrast extravasation as a separate
category and those with a persistent lling defect and total occlusion of the target
vessel. These are illustrated in Table5.1.
NHLBI has been the predominant classication method used for peripheral
artery dissection for many years; however, some suggest that it is overly complex to
be applied in routine daily practice and may incorporate features that are not relevant to peripheral artery angioplasty. For example, extravasation of contrast may be
a very important nding in the coronary vascular bed but is usually a benign feature
of peripheral artery interventions. This led to the simplied classication system
developed specically for peripheral artery interventions by Kobayashi etal [54]. It
consists of three categories based on digital subtraction angiography (Table5.2):
group A where there was no angiographic dissection; group B, where there was
mild dissection (the width of the dissection was less than one-third of the lumen);
and group C, severe dissection, where the width of the dissection was more than
one-third of the lumen. Spiral dissection was included in group C.Its simple design
was intended to facilitate wide adoption in everyday practice; however, its lack of
detail limited its utility in differentiating features which experts recognise as having
clinical prognostic value and its use in clinical research as a method of
categorisation.
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Table 5.1 The National Heart, Lung, and Blood Institute (NHLBI) dissection classication
system of procedural coronary artery dissections [53]
Type Description Depiction
A Minor radiolucency within the lumen during
contrast injection with no persistence of contrast
after luminal clearance
B Linear dissection with parallel tracts or double
lumen, with no persistence of contrast
C Extra-luminal ‘cap’ of contrast with persistence
after clearance of luminal contrast
D Spiral-shaped dissection, usually with lling
defects within the false lumen
E New persistent lling defect in the arterial
lumen
A. Stathis et al.
F Dissection with total occlusion of the arterial
lumen and no distal antegrade ow
Table 5.2 Classication of angiographic dissections after balloon angioplasty for supercial
femoral artery disease
Category Degree of dissection
A No angiographic dissection
B The width of the dissection was less than one-third of the lumen
C The width of the dissection is more than one-third of the lumen, or there is a spiral
dissection
From Kobayashi etal. [54]
Classication Systems: Intravascular Ultrasound (IVUS)
Angiographic assessment of peripheral arteries during percutaneous intervention
has several limitations. It relies upon a two-dimensional image of the arterial
lumen. The detail of the blood vessel wall is limited to calcication and contrast
entering a false lumen even with multiple orthogonal views. It provides little detail
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of plaque morphology, is challenged in the evaluation of thrombus and often
underestimates blood vessel diameter and also the presence/severity of dissection itself.
The use of IVUS as an adjunctive imaging modality has grown in popularity
since the 1990s. It provides information not available from angiography and is particularly useful in the evaluation of dissection, where it gives an accurate determination of depth and degree of arterial injury. Moreover, high-resolution IVUS can
visualise the nature of material which is compromising the lumen, to differentiate
between plaque, thrombus and intramural haematoma.
A Dutch study investigated the use of IVUS for the evaluation of dissection,
performing both qualitative and quantitative analyses [55]. The qualitative analysis
evaluated vascular wall damage, classifying the degree of injury as atherosclerotic
plaque radial tear of the intimal surface, dissection (a radial tear separating the
lesion from the underlying arterial wall) and/or medial rupture. The extent of dissection was then quantied and classied into one of the four groups (absent, minor,
moderate and severe) as determined by 30° incremental arcs of the blood vessel
circumference in cross section (Table 5.3). While this system provides a good
framework to classify the degree and extent of dissection, it is limited in its description of other features thought to be clinically important, such as length, luminal
diameter reduction and spiral morphology.
The more contemporary iDissection grading system is an alternative IVUSbased method proposed by Shammas etal. in 2018 [56]. It consists of six dissection grades which combine depth of injury (from the intima to adventitia) with
circumference of dissection (<180° or ≥180°), features known to inuence clinical outcomes (Table5.4). However, those authors acknowledged that the grading
system did not consider the length of the dissection and the presence of thrombus.
Table 5.3 Classication of dissections in femoropopliteal arteries after balloon angioplasty
Dissection Extent of dissection as assessed by IVUS
Absent No dissection
Mild 30°–90° arc of the circumference involved
Moderate 120°–180° arc of the circumference involved
Severe 210°–360° arc of the circumference involved
Adapted from Van der Lugt etal. [55]
Table 5.4 The iDissection classication scheme
Dissection Circumference <180° Circumference ≥180°
Intima A1 A2
Media B1 B2
Adventitia C1 C2
Adapted from Shammas etal. [56]
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It also failed to include spiral morphology and ow; however, it is a practical system that has the potential for wide adoption. The authors recommended a large,
prospective registry to determine its role in predicting outcomes after arterial
intervention.
While IVUS has been shown to identify dissections at higher frequency and in
greater detail than conventional angiography, it is not available to all interventionalists and is more challenged in considering ow patterns, and its interpretation
requires both skill and experience [36, 57]. It is therefore not universally applicable
and is likely to remain an adjunctive imaging modality for the foreseeable future. It
is our view that we will continue to rely on an angiographic classication system for
dissection, one that is developed for peripheral arteries, underscored by expert opinion and validated as a predictor of clinical outcomes.
A. Stathis et al.
The DiSForM Classication System
The DiSForM (Diameter reduction, Spiral shape, Flow impairment or adverse
Morphology) classication system was developed as a practical, universally applicable, angiography-based method of categorising arterial dissection designed specically for peripheral arteries. It was developed utilising a three-stage Delphi
consensus panel of experts to rst determine angiographic features of clinical
importance and then rank them for signicance. Subsequently, a treatment algorithm was designed to assist interventionalists in managing angioplasty-induced
dissection.
The features identied were luminal diameter reduction of ≥50%, spiral conguration, degree of ow impairment (by developing the FLIPI (FLow Impairment in
Peripheral Intervention) grading system) and adverse morphology (length ≥2cm
and/or multiple dissections). The DiSForM classication system was based on the
consensus of 17 expert interventional radiologists, interventional cardiologists, vascular surgeons and vascular medicine specialists who were asked to rate a series of
combined dissection features for their likelihood to lead to acute occlusion and/or
restenosis (Table 5.5). This then gives each individual dissection a pathological
classication (DxSxFxMx) which can be used to aid treatment planning and evaluation, prognosis prediction, information exchange and the ongoing investigation of
peripheral artery dissections. This classication system has features similar to the
TNM system which is in common use for the classication of malignant tumors
[58]. Examples of peripheral dissections classied using DiSForM are given in
Fig.5.2.
In the nal Delphi round, the results of all possible DxSxFxMx combinations were
collated and analysed to validate its use as a decision-making tool and provide a
treatment algorithm, which is given in Fig.5.3.
D
D
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Table 5.5 The DiSForM (Diameter reduction, Spiral shape, Flow impairment or adverse
Morphology) classication system for peripheral artery dissection
DiSForM
category Parameter Description of parameter as assessed on DSA
Di Diameter
reduction
D0Diameter reduction of <50%
D1Diameter reduction of ≥50%
a
S Spiral shape S0Non spiral (linear) conguration
S1Any spiral conguration
F Flow
impairment
F0FLIPI 0: Normal antegrade ow
b
F1FLIPI 1: Reduced antegrade ow
F2FLIPI 2: Minor antegrade penetration
F3FLIPI 3: No ow-through dissected segment, only
collateral lling
M Morphology M0On single dissection <2cm length
M1Multiple <2cm length dissections OR a single
dissection ≥2cm
M2Multiple ≥2cm dissections
a
DSA digital subtraction angiography
b
FLIPI ow impairment in peripheral intervention
a
1S0F0M0
c
1S1F2M1
b
D0S0F1M
d
D1S0F3M
1
1
Fig. 5.2 (a–d) Dissection examples classied using the DiSForM classication system for peripheral artery dissections (note that ow must be rated on digital subtraction angiography and cannot
be determined by a static image)
The strengths of the DiSForM classication system are that it is broadly applicable, does not rely on the availability of IVUS, is designed by experts in peripheral
intervention specically for use in that region and requires little additional training
to incorporate into clinical practice. Future studies are planned to validate its utility
as a tool for predicting short- and mid-term clinical outcomes.
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